We have shown that, despite their increased glycolytic muscle fiber composition, myostatin deficient mice are able to perform endurance exercise without incurring muscle damage. Myostatin deficient mice are able to successfully adapt to endurance exercise by increasing oxidative enzyme activity. Myostatin deficient mice do, however, have a decrease in overall exercise capacity. We have also analyzed gene expression changes in gastrocnemius skeletal muscle with and without myostatin inhibition in a model of diabetes to determine the molecular mechanisms of myostatin regulation of muscle metabolism at the molecular level. We have shown that myostatin inhibition specifically in muscle in a mouse model of lipodystrophy prevents the accumulation of triglycerides in muscle, the development of hyperglycemia, and hyperphagia. These results suggest that increased muscle may not only help prevent diabetes, but may also regulate food intake.